Research paper topics, free example research papers

You are welcome to search thousands of free research papers and essays. Search for your research paper topic now!

Research paper example essay prompt: Ovarian Cancer - 2095 words

NOTE: The samle research paper or essay prompt you see on this page is a free essay, available to anyone. You can use any paper as a sample on how to write research paper, essay prompts or as a source of information. We strongly discourage you to directly copy/paste any essay and turn it in for credit. If your school uses any plagiarism detecting software, you might be caught and accused of plagiarism. If you need a custom essay or research paper, written from scratch exclusively for you, please use our paid research paper writing service!

.. of segments of chromosomes (particularly 3p
and 6q) in some tumors is consistent with a role
for loss of tumor suppressor genes. Recently, a
genetic linkage study of familial breast/ovary
cancer suggested linkage of disease susceptibility
with the RH blood group locus on chromosome 1p.
Allele loss involving chromosomes 3p and 6q as
well as chromosomes 11p, 13q, and 17 have been
frequently observed in ovarian cancers. Besides
allele loss, point mutations have been identified
in the tumor suppressor gene p53 located on
chromosome17p13. Deletions of chromosome 17q have
been reported in sporadic ovarian tumors
suggesting a general involvement of this region in
ovarian tumor biology.

Allelic loss of MYB and ESR
genes map on chromosome 6q near the provisional
locus for FUCA2, the locus for a-L-fucosidase in
serum. Low activity of a-L-fucosidase in serum is
more prevalent in ovarian cancer patients. This
suggests that deficiency of a-L-fucosidase
activity in serum may be a hereditary condition
associated with increased risk for developing
ovarian cancer. This together with cytogenetic
data of losses of 6q and the allelic losses at 6q
point to the potential importance of chromosome 6q
in hereditary ovarian cancer (Altchek, 208-212).
Activation of normal proto-oncogenes by either
mutation, translocation, or gene amplification to
produce altered or overexpressed products is
believed to play an important role in the
development of ovarian tumors. Activation of
several proto- oncogenes (particularly K-RAS,
H-RAS, c-MYC, and HER-2/neu) occurs in ovarian
tumors.

However, the significance remains to be
determined. It is controversial as to whether
overexpression of the HER-2/neu gene in ovarian
cancer is associated with poor prognosis. In
addition to studying proto-oncogenes in tumors, it
may be beneficial to investigate proto-oncogenes
in germ-line DNA from members of families with
histories of ovarian cancer (Barber, 323-324). It
is questionable whether inheritance or rare
alleles of the H-RAS proto-oncogene may be linked
to susceptibility to ovarian cancers. Diagnosis
and Treatment The early diagnosis of ovarian
cancer is a matter of chance and not a triumph of
scientific approach.

In most cases, the finding of
a pelvic mass is the only available method of
diagnosis, with the exception of functioning
tumors which may manifest endocrine even with
minimal ovarian enlargement. Symptomatology
includes vague abdominal discomfort, dyspepsia,
increased flatulence, sense of bloating,
particularly after ingesting food, mild digestive
disturbances, and pelvic unrest which may be
present for several months before diagnosis
(Sharp, 161-163). There are a great number of
imaging techniques that are available.
Ultrasounds, particularly vaginal ultrasound, has
increased the rate of pick-up of early lesions,
particularly when the color Doppler method is
used. Unfortunately, vaginal sonography and CA 125
have had an increasing number of false positive
examinations. Pelvic findings are often minimal
and not helpful in making a diagnosis.

However,
combined with a high index of suspicion, this may
alert the physician to the diagnosis. These pelvic
signs include: Mass in the ovarian area Relative
immobility due to fixation of adhesions
Irregularity of the tumor Shotty consistency with
increased firmness Tumors in the cul-de-sac
described as a handful of knuckles Relative
insensitivity of the mass Increasing size under
observation Bilaterality (70% for ovarian
carcinoma versus 5% for benign cases) (Barber,
136) Tumor markers have been particularly useful
in monitoring treatment, however, the markers have
and will probably always have a disadvantage in
identifying an early tumor. To date, only two,
human gonadotropin (HCG) and alpha fetoprotein,
are known to be sensitive and specific. The
problem with tumor markers as a means of making a
diagnosis is that a tumor marker is developed from
a certain volume of tumor. By that time it is no
longer an early but rather a biologically late
tumor (Altchek, 292).

Many reports have described
murine monoclonal antibodies (MAbs) as potential
tools for diagnosing malignant ovarian tumors.
Yamada et al attempted to develop a MAb that can
differentiate cells with early malignant change
from adjacent benign tumor cells in cases of
borderline malignancy. They developed MAb 12C3 by
immunizing mice with a cell line derived from a
human ovarian tumor. The antibody reacted with
human ovarian carcinomas rather than with germ
cell tumors. MAb 12C3 stained 67.7% of ovarian
epithelial malignancies, but exhibited an
extremely low reactivity with other malignancies.
MAb 12C3 detected a novel antigen whose
distribution in normal tissue is restricted.
According to Yamada et al, MAb 12C3 will serve as
a powerful new tool for the histologic detection
of early malignant changes in borderline
epithelial neoplasms. MAb 12C3 may also be useful
as a targeting agent for cancer chemotherapy
(Yamada, 293-294).

Currently there are several
serum markers that are available to help make a
diagnosis. These include CA 125, CEA, DNB/70K,
LASA-P, and serum inhibin. Recently the urinary
gonadotropin peptide (UCP) and the
collagen-stimulating factor have been added.
Although the tumor markers have a low specificity
and sensitivity, they are often used in screening
for ovarian cancer. A new tumor marker CA125-2 has
greater specificity than CA125. In general, tumor
markers have a very limited role in screening for
ovarian cancer.

The common epithelial cancer of
the ovary is unique in killing the patient while
being, in the vast majority of the cases, enclosed
in the anatomical area where it initially
developed: the peritoneal cavity. Even with early
localized cancer, lymph node metastases are not
rare in the pelvic or aortic areas. In most of the
cases, death is due to intraperitoneal
proliferation, ascites, protein loss and cachexia.
The concept of debulking or cytoreductive surgery
is currently the dominant concept in treatment.
The first goal in debulking surgery is inhibition
of debulking surgery is inhibition of the vicious
cycle of malnutrition, nausea, vomiting, and
dyspepsia commonly found in patients with mid to
advanced stage disease. Cytoreductive surgery
enhances the efficiency of chemotherapy as the
survival curve of the patients whose largest
residual mass size was, after surgery, below the
1.5 cm limit is the same as the curve of the
patients whose largest metastatic lesions were
below the 1.5 cm limit at the outset (Altchek,
422-424). The aggressiveness of the debulking
surgery is a key question surgeons must face when
treating ovarian cancers.

The debulking of very
large metastatic masses makes no sense from the
oncologic perspective. As for extrapelvic masses
the debulking, even if more acceptable, remains
full of danger and exposes the patient to a heavy
handicap. For these reasons the extra-genital
resections have to be limited to lymphadenectomy,
omentectomy, pelvic abdominal peritoneal
resections and rectosigmoid junction resection.
That means that stages IIB and IIC and stages IIIA
and IIB are the only true indications for
extrapelvic cytoreductive surgery. Colectomy,
ileectomy, splenectomy, segmental hepatectomy are
only exceptionally indicated if they allow one to
perform a real optimal resection. The standard
cytoreductive surgery is the total hysterectomy
with bilateral salpingoophorectomy.

This surgery
may be done with aortic and pelvic lymph node
sampling, omentectomy, and, if necessary,
resection of the rectosigmoidal junction (Barber.
182-183). The concept of administering drugs
directly into the peritoneal cavity as therapy of
ovarian cancer was attempted more than three
decades ago. However, it has only been within the
last ten years that a firm basis for this method
of drug delivery has become established. The
essential goal is to expose the tumor to higher
concentrations of drug for longer periods of time
than is possible with systemic drug delivery.
Several agents have been examined for their
efficacy, safety and pharmacokinetic advantage
when administered via the peritoneal route.
Cisplatin has undergone the most extensive
evaluation for regional delivery. Cisplatin
reaches the systemic compartment in significant
concentrations when it is administered
intraperitoneally.

The dose limiting toxicity of
intraperitoneally administered cisplatin is
nephrotoxicity, neurotoxicity and emesis. The
depth of penetration of cisplatin into the
peritoneal lining and tumor following regional
delivery is only 1 to 2 mm from the surface which
limits its efficacy. Thus, the only patients with
ovarian cancer who would likely benefit would be
those with very small residual tumor volumes.
Overall, approximately 30 to 40% of patients with
small volume residual ovarian cancer have been
shown to demonstrate an objective clinical
response to cisplatin-based locally administered
therapy with 20 to 30% of patients achieving a
surgically documented complete response. As a
general rule, patients whose tumors have
demonstrated an inherent resistance to cisplatin
following systemic therapy are not considered for
treatment with platinum-based intraperitoneal
therapy (Altchek, 444-446). In patients with small
volume residual disease at the time of second look
laparotomy, who have demonstrated inherent
resistance to platinum-based regimens, alternative
intraperitoneal treatment programs can be
considered.

Other agents include mitoxantrone, and
recombinant alpha-interpheron. Intraperitoneal
mitoxanthone has been shown to have definite
activity in small volume residual
platinum-refractory ovarian cancer. Unfortunately,
the dose limiting toxicity of the agent is
abdominal pain and adhesion formation, possibly
leading to bowel obstruction. Recent data suggests
the local toxicity of mitoxanthone can be
decreased considerably by delivering the agent in
microdoses. Ovarian tumors may have either
intrinsic or acquired drug resistance.

Many
mechanisms of drug resistance have been described.
Expression of the MDR1 gene that encodes the drug
efflux protein known as p-glycoprotein, has been
shown to confer the characteristic multi-drug
resistance to clones of some cancers. The most
widely considered definition of platinum response
is response to first-line platinum treatment and
disease free interval. Primary platinum resistance
may be defined as any progression on treatment.
Secondary platinum resistance is the absence of
progression on primary platinum-based therapy but
progression at the time of platinum retreatment
for relapse (Sharp, 205-207). Second-line
chemotherapy for recurrent ovarian cancer is
dependent on preferences of both the patient and
physician. Retreatment with platinum therapy
appears to offer significant opportunity for
clinical response and palliation but relatively
little hope for long-term cure.

Paclitaxel (trade
name: Taxol), a prototype of the taxanes, is
cytotoxic to ovarian cancer. Approximately 20% of
platinum failures respond to standard doses of
paclitaxel. Studies are in progress of dose
intensification and intraperitoneal administration
(Barber, 227-228). This class of drugs is now
thought to represent an active addition to the
platinum analogs, either as primary therapy, in
combination with platinum, or as salvage therapy
after failure of platinum. In advanced stages,
there is suggestive evidence of partial
responsiveness of OCCA to radiation as well as
cchemotherapy, adriamycin, cytoxan, and
cisPlatinum-containing combinations (Yoonessi,
295).

Radiation techniques include intraperitoneal
radioactive gold or chromium phosphate and
external beam therapy to the abdomen and pelvis.
The role of radiation therapy in treatment of
ovarian canver has diminished in prominence as the
spread pattern of ovarian cancer and the normal
tissue bed involved in the treatment of this
neoplasm make effective radiation therapy
difficult. When the residual disease after
laparotomy is bulky, radiation therapy is
particularly ineffective. If postoperative
radiation is prescribed for a patient, it is
important that theentire abdomen and pelvis are
optimally treated to elicit a response from the
tumor (Sharp, 278-280). In the last few decades,
the aggressive attempt to optimize the treatment
of ovarian clear cell adenocarcinoma and ovarian
cancer in general has seen remarkable improvements
in the response rates of patients with advanced
stage cancer without dramatically improving
long-term survival. The promises of new drugs with
activity when platinum agents fail is encouraging
and fosters hope that, in the decades to come, the
endeavors of surgical and pharmacoogical research
will make ovarian cancer an easily treatable
disease.